Research Uncovers Why Some Cancer Therapies Fail

MIT study finds cancer cells can activate backup survival pathways to resist targeted therapies.

Mar. 27, 2026 at 2:08am

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Drugs that block enzymes called tyrosine kinases are among the most effective targeted therapies for cancer, but they typically only work for 40 to 80 percent of patients. MIT researchers have discovered that many of these tumors have turned on a backup survival pathway that helps them keep growing when the targeted pathway is blocked, allowing the cells to be resistant to a wide variety of therapies. The researchers found that treating the resistant cells with both a tyrosine kinase inhibitor and a drug that targets the backup pathway led to much greater cell death.

Why it matters

This research helps explain why some cancer patients don't respond to targeted therapies, and suggests a potential solution by combining tyrosine kinase inhibitors with drugs that target the backup survival pathways. Understanding the mechanisms behind drug resistance could lead to more effective cancer treatments and better outcomes for patients.

The details

The MIT team examined six different cancer cell lines, including those with EGFR, MET, and ALK mutations. They found that even in resistant cells, the drugs did knock out signaling by their target kinase. However, an alternative network regulated by SRC family kinases was already turned on in the resistant cells, helping them survive the treatment. Treating the resistant cells with both a tyrosine kinase inhibitor and an SRC inhibitor led to much greater cell death.

  • The study was published on March 27, 2026.

The players

Forest White

The Ned C. and Janet C. Rice Professor of Biological Engineering at MIT and the senior author of the study.

Cameron Flower

The lead author of the paper, who is now a postdoc at Dana-Farber Cancer Institute and Boston Children's Hospital.

Benjamin Neel

A professor of medicine at NYU Grossman School of Medicine, who was not involved in the study but commented on the findings.

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What they’re saying

“This seems to be hardwired into the cells and seems to be providing activation of a critical survival pathway in cancer cells. This pathway allows the cells to be resistant to a wide variety of therapies, including chemotherapies.”

— Forest White, The Ned C. and Janet C. Rice Professor of Biological Engineering at MIT

“As inhibitors for SRC kinases are also drugs, the work suggests that combining inhibitors of driver oncogenes with SRC inhibitors could increase the number of patients who would benefit. This strategy merits testing in new clinical trials.”

— Benjamin Neel, Professor of medicine at NYU Grossman School of Medicine

What’s next

Clinical trials are now underway to test the combination of a tyrosine kinase inhibitor and an SRC inhibitor in lung cancer patients. The MIT team hopes to work with the same drug company to run a similar trial in pancreatic cancer patients.

The takeaway

This research provides important insights into the mechanisms behind drug resistance in cancer, and suggests a promising new approach of combining targeted therapies with drugs that inhibit backup survival pathways. If successful in clinical trials, this strategy could significantly improve outcomes for cancer patients whose tumors are resistant to current targeted therapies.